Functionally similar genes exhibit comparable/similar time-course expression kinetics in the UV-induced photoaged mouse model.

Skin photoaging induced by ultraviolet (UV) irradiation contributes to the formation of thick and coarse wrinkles. Humans are exposed to UV light throughout their lives. Therefore, it is crucial to determine the time-sequential effects of UV on the skin.

Melia azedarach extract stimulates melanogenesis through increase of tyrosinase-related protein 1 expression in B16F10 mouse melanoma cells.

Melia azedarach (MA) has been used in folk medicine in Asia for the treatment of several diseases. Several constituents from MA possess anti-herpetic, anti-angiogenic and anticancer properties. The aim of the present study was to investigate the effect of a 70% ethanol extract of MA on melanogenesis and the underlying mechanisms involved.

Ardisia crenata extract stimulates melanogenesis in B16F10 melanoma cells through inhibiting ERK1/2 and Akt activation.

Melanin protects the skin against ultraviolet radiation by scattering incoming light and absorbing diverse free radicals. Agents that increase melanin synthesis in melanocytes may reduce the risk of photodamage and skin cancer. The present study investigated the effect of a methanol extract of Ardisia crenata (AC) on melanogenesis in B16F10 cells.

[6]-Shogaol inhibits melanogenesis in B16 mouse melanoma cells through activation of the ERK pathway.

Aim: To investigate the effect of [6]-shogaol, an active ingredient in ginger, on melanogenesis and the underlying mechanisms.

Methods: B16F10 mouse melanoma cells were tested. Cell viability was determined with the MTT assay.

Estrogen receptor beta is a novel therapeutic target for photoaging.

One of the many harmful factors faced by the skin is solar UV radiation, which damages skin by inducing chronic low-grade inflammation through increased expression of proinflammatory cytokines, metalloproteinases (MMPs) and cyclooxygenase-2 (COX-2). Estrogen receptors (ERs) alpha and beta are ligand-dependent transcription factors that are expressed in skin, and an ERbeta agonist has previously shown efficacy in vivo in models of pain and inflammation. Because ERbeta does not carry the breast and uterine proliferation liabilities of ERalpha, we decided to explore the possibility of using ERbeta as a target for photoaging.